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Dr Cenci Nilsson has pioneered the development of pre-clinical models mimicking different features of Parkinson’s disease (in particular, levodopa-induced dyskinesia and akinesia). She heads the Basal Ganglia Pathophysiology Laboratory at Lund University, Sweden. Her current research is directed towards discovering new symptomatic and neurorestorative/neuroprotective treatments for Parkinson’s disease.

Parkinson’s podcast: L-dopa – waiting for the next act

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Author: Geoffrey ChangPublished: 18 February 2016

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Why has it taken so long to improve levodopa – AKA L-dopa – delivery so that Parkinson’s patients can experience the drug’s benefit in a more continuous fashion?

In the latest Portland Countdown podcast, regular hosts Dave Iverson and Jon Palfreman invite special guest Dr Angela Cenci Nilsson to discuss how the landscape has changed since levodopa, or ‘dopamine-replacement’ therapy, was first developed 50 years ago – and today’s prospects for what was the first major breakthrough in Parkinson’s treatments.

While it’s undoubtedly a life-changing help for patients, levodopa isn’t a cure. The podcast explores why it has taken so long to improve its effectiveness or to develop the next breakthrough treatment. The panel also discuss the challenges of convincing big pharmaceutical companies to invest in these types of treatments.

The aim of the Portland Countdown series is to give listeners new perspectives on the latest advances in Parkinson’s research and treatment.

The shows, developed by the World Parkinson Coalition, are aired online on the first Tuesday of every month from June 2015 to September 2016 – when the 4th World Parkinson Congress takes place in Portland, Oregon, US. The podcasts are free and available for download.

The full schedule of show topics and guest speaker profiles is available here

Share this story

Dr Cenci Nilsson has pioneered the development of pre-clinical models mimicking different features of Parkinson’s disease (in particular, levodopa-induced dyskinesia and akinesia). She heads the Basal Ganglia Pathophysiology Laboratory at Lund University, Sweden. Her current research is directed towards discovering new symptomatic and neurorestorative/neuroprotective treatments for Parkinson’s disease.

IN THE NEWS

Carefully selected news stories from the international Parkinson's community.

3 weeks ago

Excess calcium in brain could cause Parkinson’s

Researchers at the University of Cambridge, UK, have discovered that excess levels of calcium in brain cells may lead to the formation of the toxic clusters that signify Parkinson’s disease. The findings, reported in the journal ‘Nature Communications’, show that calcium can influence the interaction between small membranous structures inside nerve endings, which are important for neuronal signaling in the brain, and alpha-synuclein – the protein associated with Parkinson’s disease. Dr Janin Lautenschläger, the paper’s first author, said: “This is the first time we’ve seen that calcium influences the way alpha-synuclein interacts with synaptic vesicles. We think that alpha-synuclein is almost like a calcium sensor. In the presence of calcium, it changes its structure and how it interacts with its environment, which is likely very important for its normal function.”

Jewish people with Crohn’s disease more likely to carry LRRK2 gene mutation

A scientific study has concluded that there may be a link between Parkinson’s and Crohn’s disease within the Ashkenazi Jewish community. The study’s findings, which were published in the journal ‘Science Translational Medicine’, has found that members of the population with Crohn’s disease are more likely to carry the LRRK2 mutation which is a significant cause of Parkinson’s. Lead researcher Dr Inga Peter, professor of genetics and genomic sciences at the Icahn School of Medicine, New York, US, said: “Crohn’s disease is a complex disorder with multiple genes and environmental factors involved, which disproportionately affects individuals of Ashkenazi Jewish ancestry. “The presence of shared LRRK2 mutations in patients with Crohn’s disease and Parkinson’s disease provides refined insight into disease mechanisms and may have major implications for the treatment of these two seemingly unrelated diseases.”

Could caffeine in the blood help diagnose Parkinson’s?

Blood caffeine levels could be promising diagnostic biomarkers for early-stage Parkinson’s, Japanese researchers reported in the journal ‘Neurology’ earlier this month. The study found that people with Parkinson’s had lower levels of caffeine and caffeine metabolites in their blood than people without the disease, at the same consumption rate. Caffeine concentrations also were decreased in Parkinson’s patients with motor fluctuations than in those without Parkinson’s. However, patients in more severe disease stages did not have lower caffeine levels. The study’s authors, Dr David Munoz, University of Toronto, and Dr Shinsuke Fujioka, Fukuoka University, suggested that the “decrease in caffeine metabolites occurs from the earliest stages of Parkinson’s.” They added: “If a future study were to demonstrate similar decreases in caffeine in untreated patients with Parkinson’s […] the implications of the current study would take enormous importance.”